Burns And Wound Healing Flashcards

1
Q

Remarks on smoke inhalation injury

A

Hydrogen cyanide toxicity may be a component
-tx:
»SODIUM THIOSULFATE: transforms cyanide into a nontoxic thiocyanate derivative, but it works slowly and is not effective for acute therapy
»HYDROXOCOBALAMIN: quickly complexes with cyanide and is excreted by the kidney; recommended for IMMEDIATE THERAPY
»100% oxygen: helps resolve lactic acidosis

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2
Q

Which is a common sequelae of electrical injury

A

Cataracts

  • occur in 5-7% of patients
  • frequently bilateral
  • typically manifest within 1 -2 eyars of injury
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3
Q

Remarks on silver sulfadiazine

A

Destroys skin grafts and is contraindicated on burns or donor sites in proximity to newly grafted areas
It may also retard epithelial migration in healing partial thickness wounds

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4
Q

Remarks on mafenide acetate

A

DOC for burn eschar penetration

Carbonic anyhydrase inhibitor

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5
Q

Remarks on nutrition in burn patients

A

Baseline metabolic rate increase by as muchh as 200%
Early enteral feeding for px with burns >20%TBSA is safe.
*harris-Benedict equation: gender, age, height, weight; inaccurate in burns <40%
*curreri formula: 25kcal/kg/day + 40 kcal/%TBSA/day

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6
Q

3 days after admission, burn wound biopsy shows 10^4 Pseudomonas organism per gram of tissue. What to do?

A

Start subeschar clysis with antibiotics

  • systemic antibiotics usually are ineffective at this point because by the 3rd day after a burn, blood flow to a burn wound is markedly decreased
  • once coloniatiotn of a burn has occurred, surgical excision is EXTREMELY DANGEROUS, as systemic seeding will occur
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7
Q

PE: central vevnous catheter insertion site was red, tender, and warm. What to do?

A

Removal of central venous catheter, culture tip, and placement of new catheter on contralateral site

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8
Q

Remarks on PMNs and wound healing

A

First infiltrating cells
Peaks at 24-48 hours
Release proteases such as collagenases, which participate in matrix and ground substance degradation in the early phse of wound healing.
They DO NOT appear to play a role in collagen deposition or acquisition of mechanical wound strength
On the contrary, neutrophil factors have been implicated in delaying the epithelial closure of wounds

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9
Q

The proliferative phase of wound healing occurs how long after injury?

A

7 days
Roughly spans days 4 through 12
Tissue continuity is reestablished

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10
Q

Strongest chemotactic factor for fibrobalst

A

Platelet derived growth factor (PDGF)

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11
Q

Stages of wound healing

A

Hemostasis and inflammation (D0-6)
Proliferation (D4-12)
Maturation and remodeling (D8-6-12months)

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12
Q

Peak of macrophages

A

48-96 hours

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13
Q

Remarks on T cells

A

Peak 1 week Post-injury

bridge transition from inflammation to proliferative phase

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14
Q

Final step in establishing tissue integrity

A

Epithelialization (48 hours)

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15
Q

Remarks on matrix

A

Earliy matrix: fibronectin and collagen type III
Next matrix: GAGs and proteoglycans
FINAL MATRIX: COLLAGEN TYPE I

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16
Q

Fibrillin

A

A glycoprotein secreted by fibroblasts

Essential for the formation of elastic fibers found in connective tissue

17
Q

Over half of the EDS patients manifest genetic defects encoding

A

alpha chains of collagen type V ✅ (Schwartz)

—> CLASSIC EDS

18
Q

Classic EDS phenotypic findings

A
Thin, firable skin with prominent viens
Easy bruising
Poor wound healing
Atrophic scar formation
Recurrent hernia
Hyperextensible joint
19
Q

GI problems of EDS

A

Bleeding
Hiatal hernia
Intestinal diverticula
Rectal prolapse

20
Q

Vessel problems of EDS

A

Fragile small blood vessels

Large vessesl may develop aneurysms, varicosities, AV fistulas, spontaneous rupture

21
Q

Remarks on marfan’s syndrome

A

Also prone to hernias

Skin may be hyperextensible, but shows NO DELAY in wound healing

22
Q

When a long bone fracture is repaired by internal fixaion with plates and screws…

A

Direct bone-to-bone healing occurs without soft callus formation and endochondral ossification (which are characteristic of closed frcture mgt)
HOWEVER, internal reduction does NOT prevent delayed union, eespecially when oinfection or poor blodd supply are present

23
Q

Impartes the greates tensile strength of GI tract

A

Submucosal layer, composed of abundant collagenous and elastic fibers

24
Q

Collagen synthesis in the GI tract is carried out by

A

Both fibroblasts and smomoth muscle cells

25
Q

Watertight seal of GI tract is due to

A

Serosal healing

26
Q

Steroid-delayed healing of cutaneous wounds can be stimulated to epithelialize by

A

Topical application of vitamin A

27
Q

What type of nerve injury involves disruption of axonal continuity with preserved Schwann cell basal lamina

A

Axonotmesis

28
Q

3 types of nerve injuries

A

NEUROPRAXIA (focal demyelination)
AXONOTMESIS (interruption of axonal continuity but preservaitaon of Schwann cell basal lamina)
NEUROTMESIS (complete transection)

29
Q

Wallerian degeneration

A

Phagocytes remove the degenerating axons and myelin sheath from the distal stump

30
Q

The major cause of impaired wound healing is

A

Local tissue infection

31
Q

Supplementation of which of the ff micronutrients improves wound healing in patients without micronutriennt deficiency

A

Vitamin A

  • increases lability of lyososomal membranes
  • increases influx of macrophages
  • directly increases collagen production and epidermal growth factor receptors
  • reverse the inhibitory effects of steroids on wound healing
  • in the severely injured patient, supplemental doses of vitamin A have been recommended. Doses ranging from 25,000 to 100,00 IU/day have been advocated.
32
Q

Which type of collagen is most important in wound healing

A

Type III

33
Q

Zinc and wound healing

A

To date, no study has shown improved wound healing with zinc supplementation in patients who are not zinc deficient (2016)

34
Q

Remarks on cartilage healing

A

Avascular and depends on diffusion of nutrients across thhe matrix
Additionally, the hypervascular periCHONDRIUM contributes substantially to the nutrition of the crtilage

35
Q

Signs of malignant transforamtion in a chronic wound include

A

Overturned wound edges

36
Q

Treatment of choice for keloids

A

Excision PLUS adjuvant therapy (e.g. radiation, intralesionsal steroid injection, topical application of silicone sheets)
*excision alone is subject 45-100% recurrence

37
Q

Remarks on peritoneal adhesions

A

Occur in 67% of px with prior surgical procedures
Occur in 28% of px with hx of intra-abdominal infection
Following rectal, left colectomy, or total colectomy, SBO 11% within 1 year, and 30% by 10 years

38
Q

Which growth factor has been formulated and approved for treatment of diabetic foot ulcers?

A

PDGF-BB

-increases incidence of total healing and decreases healing time